Background: This experiment was conducted to test the hypothesis that vitamin E(Vit E) and acetylsalicylic acid(ASA), a cyclooxygenase-2(COX-2) inhibitor, will additively reduce the production of the immunosuppressive...Background: This experiment was conducted to test the hypothesis that vitamin E(Vit E) and acetylsalicylic acid(ASA), a cyclooxygenase-2(COX-2) inhibitor, will additively reduce the production of the immunosuppressive molecule prostaglandin E_2(PGE_2) and hence reduce inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of E. coli.Methods: The experiment was conducted in a research facility with 192 individually-housed male weaner pigs(Landrace × Large White) weighing 6.6 ± 0.04 kg(mean ± SEM). The pigs were experimentally infected with an enterotoxigenic strain of E. coli and were allocated to a 2 × 3 factorial design with the respective factors being without and with 125 ppm ASA and three levels of Vit E supplementation(50, 100 or 200 IU/kg diet, dl-α-tocopheryl acetate).Results: Acetylsalicylic acid supplementation improved average daily gain(P < 0.05) and tended to improve feed:gain ratio(P < 0.10) during the first 14 d after weaning. Acetylsalicylic acid supplementation also improved(P < 0.001) amino acid utilization efficiency(as assessed by plasma urea level) and tended to decrease(P < 0.10) PGE_2 production in the liver without affecting smal intestinal histology and tight junction protein mR NA expression in the jejunal epithelium. Vitamin E supplementation greater than 100 IU/kg diet sustained both the plasma Vit E concentration(P < 0.001) and plasma haptoglobin content(P < 0.001) after weaning. However, there was no additive effects of the combined supplementation of ASA and Vit E on performance, intestinal barrier function and inflammatory responses of weaned pigs.Conclusions: Although ASA and vitamin E improved amino acid utilization efficiency and reduced acute inflammatory responses, ASA and vitamin E did not additively reduce production of PGE_2 and inflammatory responses in weaner pigs experimental y infected with an enterotoxigenic strain of E. coli.展开更多
基金support by Australian Cooperative Research Centre for High Integrity Australian Pork(Award number 2C-110 1213)
文摘Background: This experiment was conducted to test the hypothesis that vitamin E(Vit E) and acetylsalicylic acid(ASA), a cyclooxygenase-2(COX-2) inhibitor, will additively reduce the production of the immunosuppressive molecule prostaglandin E_2(PGE_2) and hence reduce inflammatory responses in weaner pigs experimentally infected with an enterotoxigenic strain of E. coli.Methods: The experiment was conducted in a research facility with 192 individually-housed male weaner pigs(Landrace × Large White) weighing 6.6 ± 0.04 kg(mean ± SEM). The pigs were experimentally infected with an enterotoxigenic strain of E. coli and were allocated to a 2 × 3 factorial design with the respective factors being without and with 125 ppm ASA and three levels of Vit E supplementation(50, 100 or 200 IU/kg diet, dl-α-tocopheryl acetate).Results: Acetylsalicylic acid supplementation improved average daily gain(P < 0.05) and tended to improve feed:gain ratio(P < 0.10) during the first 14 d after weaning. Acetylsalicylic acid supplementation also improved(P < 0.001) amino acid utilization efficiency(as assessed by plasma urea level) and tended to decrease(P < 0.10) PGE_2 production in the liver without affecting smal intestinal histology and tight junction protein mR NA expression in the jejunal epithelium. Vitamin E supplementation greater than 100 IU/kg diet sustained both the plasma Vit E concentration(P < 0.001) and plasma haptoglobin content(P < 0.001) after weaning. However, there was no additive effects of the combined supplementation of ASA and Vit E on performance, intestinal barrier function and inflammatory responses of weaned pigs.Conclusions: Although ASA and vitamin E improved amino acid utilization efficiency and reduced acute inflammatory responses, ASA and vitamin E did not additively reduce production of PGE_2 and inflammatory responses in weaner pigs experimental y infected with an enterotoxigenic strain of E. coli.
